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28 Cards in this Set

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  • Back
What are the glucose transporters?
--In all mammalian cells
--Easily saturated (Km=1), so not good for high glucose concentrations.

--In liver and pancreatic B cells
--Not easily saturated (Km=15-20), so great for liver and pancreas, where glucose is high

--In all mammalian cells

--In muscle/fat cells

--In small intestine.
What is role of glycolysis in liver?
--Energy source
--Lipid precursors (glucose-->fat)
--Glycogen source--First step in glycolysis is also step in glycogen synthesis.
What is role of glycolysis in muscle?
--Energy source
--Glycogen source--First step in glycolysis is also step in glycogen synthesis.
What is role of glycolysis in adipose?
--Energy source.
--lipid precursors (glucose-->fat)
What is role of glycolysis in brain?
--Practically only source of energy
--Lipid precursors (glucose-->fat)
What is role of glycolysis in RBCs?
--ONLY energy source--can't use anything else!
What is role of glycolysis in other tissues?
--Lipid precursors (glucose-->fat)
What are the steps in glycolytic pathway?
"PREPPING" the sugar--

glucose--(hexokinase)-->G-6-P--(phosphoglucose isomerase)-->F-6-P--(PFK-1)-->F-1,6-bisP

"SPLITTING" the sugar

F-1,6-bisP--(fructose bisphosphate aldolase)-->SPLIT into glyceraldehyde-3-phosphate (G-3-P) AND DHAP (not useful--must be converted to G-3-P by triose phosphate isomerase


G-3-P--(G-3-P dehydrogenase)-->1,3-bisphosphoglycerate--(phosphoglycerate kinase)-->3 phosphoglycerate--(phosphoglycerate mutase)-->2-phosphoglycerate-->phosphoenolpyruvate--(pyruvate kinase)-->Pyruvate

if anaerobic...
What is regulation of glycolysis using glucose transporters?
--Adipose/muscle possess GLUT-4 transporter-->movement to membrane stimulated by insulin-->will increase GLUT-4 transporters-->more glucose comes in-->more glycolysis.
What is regulation of glycolysis using Glucose phosphorylation?
--phosphorylates glucose in muscle-->forms G-6-P
--Inhibited by G-6-P--feedback inhibition!
--If PFK-1 or PK are inhibited, G-6-P increases-->inhibits hexokinase-->inhibits glycolysis. This is what occurs in fasting.

Glucokinase (GK)
--phosphorylates glucose in liver-->forms G-6-P
--Active only when glucose is high--good, because, when glucose is low, will NOT be active--save glucose for RBC's and brain.
What are some features of glucokinase (GK)?
--GK has lower glucose affinity than hexokinase--insulin release/liver glycolysis increases in fed state and decrease in fasting state--hexokinase is saturated easily, so less difference b/w states.
--GK is activated by glucose--inactive when glucose is low--keeps glycolysis off.
--GK is induced by insulin--when insulin is low, GK is inactive (good, because only active during fed state)

...Overall, shows you that the FIRST step in liver glycolysis will be ACTIVE in FED state, but OFF in FASTING state.
How is glycolysis regulated by PFK-1?
--PFK-1 is the rate-limiting step in glycolysis.
--INHIBITED by: ATP, citrate, protons.
--Fed state-->prevents excess fat production by glycolysis.
--Fasting state-->don't need glycolysis--using B-oxidation--saving glucose for brain, RBC's.

AMP, F-2,6-bisP
AMP--shows cell needs more energy/glycolysis
Describe glycolysis inhibition by glucagon thru F-2,6-bisP
--PFK-2 is a dual kinase/phosphatase that converts F-6-P-->F-2,6-BisP
--F-2,6-BisP activates PFK-1-->activates glycolysis.
-->to INHIBIT glycolysis-->want to turn off KINASE (less F-2,6-BisP) and turn on PHOSPHATASE (F-2,6-bisP-->F-6-P)
--SO, glucagon binds receptor->activates adenylate cyclase-> activates cAMP->activates protein kinase A->phosphorylates PFK-2->activates PHOSPHATASE and inhibits KINASE-->decreases F-2,6-bisP levels-->PFK-1 is not activated->less glycolysis.
What happens to PFK-2 when insulin increases again?
-->a phosphatase is activated-->PFK-2 de-phosphorylated-->KINASE activated again
-->also can lower cAMP levels-->decrease PKA-->lead to dephosphorylation of enzyme-->increases KINASE activity and decreases PHOSPHATASE activity-->increases F-2,6-bisP-->increase PFK-1 activity-->increases glycolysis!
How is PFK-2 activation/inhibition handled in the muscle?
Remember--in muscle, epinephrine increases glycolysis (need energy when you work out)
--So, instead of INHIBITING PFK-2, Epi activates it-->stimulating F-2,6-bisP production.
-->Epi uses same receptor mechanism as glucagon, so would expect the same reaction..
-->Why? Because PFK-2 in muscle is an ISOFORM--phosphorylation by PKA actually DECREASES PHOSPHATASE activity and INCREASES KINASE activity.
How is glycolysis regulated by pyruvate kinase (PK)?
--INHIBITED by ATP and alanine.
--shows that energy needs are being met in the cell.
ATP--plenty of energy--don't need glycolysis
Alanine--shows gluconeogenesis is happening--don't need glycolysis.
--FASTING (don't want glycolysis)-->cAMP-->PKA-->PHOSPHORYLATES PK-->inactivates it
--FED (want glycolysis)-->insulin-->phosphatase-->DEPHOSPHORYLATES PK-->activates it.
What is importance of 2, 3 bisphosphoglycerate (2,3-BPG)?
RBC's require 2,3-BPG to bind O2 to hemoglobin.
--RBC's have enzymes that allow it to be generated from glycolytic intermediates.

1/2 glucose-->1, 3 BPG--(2,3-BPG mutase)-->2,3-BPG--(2,3 BPG phosphatase)-->re-enters glycolysis as 3-phosphoglycerate

--"sneaks" in at the very end of glycolysis
*bypassing ATP producing reactions.
How does fructose get into glycolysis?
Liver makes fructokinase

Fructose--(fructokinase)-->F-1-P--(aldolase B)-->glyceraldehyde--(triose kinase)-->G-3-P-->lactate OR DHAP

--BYPASSES the regulated PFK-1 step (F-6-P-->F-1,6-BisP)
How does galactose get into glycolysis?

Galactose-1-P + UDP-glucose--(galactose-1-phosphaste uridyl transferase)-->UDP-galactose (w/uridine) + GLUCOSE-1-P--(UDP-galactose-4-epimerase)-->UDP-glucose

GLUCOSE-1-P converted to G-6-P by phosphoglucomutase-->can enter glycolysis
How does glycerol get into glycolysis?
Glycerol--(glycerol kinase)-->Glycerol phosphate--(glycerol phosphate dehydrogenase)-->DHAP
What is pyruvate kinase deficiency?
--Type of hexoase metabolism disorder.
--leads to anemia.
What is Warburg phenomenon?
--type of hexose metabolism disorder
--when tumor forms, it has no blood supply
--must survive by glycolysis and TF's
What is galactosemia?
--No galactokinase
--accumulation of galactose--(aldose reductase)-->galacticol-->osmotically active-->cataracts!
What is uridyl transferase deficiency?
--no uridyl transferase
--accumulate galactose, galactose-1-P
--get cataracts, but gal-1-P is toxic-->failure to thrive
What is fructose intolerance?
--Deficiency of fructokinase--not too bad--extra-hepatic tissues can metabolize fructose using hexokinase.
--Deficiency of aldolase B--more serious, because blocks metabolism of F-1-P-->accumulation of F-1-P ties up phosphate-->decreases ATP-->degradation of accumulated AMP can worsen gout.
-->also, F-1-P is toxic to liver.
What is fructose toxicity?
--ingestion of large amounts of fructose.
--Bypass PFK-1 step (stated earler)
--Excess fructose-->converted to fat
-->although F-1-P can be metabolized, it still accumulates-->leads to fructose intolerence.
How are carbohydrates digested/absorbed?
Breaking down POLYsaccharides (starch, glycogen) and DIsaccharides (lactose, sucrose) into MONOsaccharides (galactose, glucose, fructose)


-->SUCROSE and LACTOSE also enter at this step.






FRUCTOSE-->favorable conc. gradient, so transported passively by Glut-5 and Glut-2

GLUCOSE/GALACTOSE-->NOT favorable conc. gradient. "Piggy-back" w/ sodium on the sodium-glucose transporter (SGLT1)--moves Na+ back into cell after being pumped out by Na/K pump
What are disaccharide deficiencies?
Lactase deficiency-->lactose intolerence
SGLT-1 deficiency-->impair glucose/galactose absorption.